However, the ΔNp63α mice are more susceptible to mutagen-induced tumor initiation and progression, and in vitro analyses demonstrated a delay in senescence with increased p53, Sirt1, and Lsh, and suppressed p16INK4A and p19ARF levels [60], consistent with established roles of ΔNp63α as a contributor to carcinogenesis [90,92]. The gene discussed is CDKN2A; the disease is neoplasm.